A cell cycle and nutritional checkpoint controlling bacterial surface adhesion.

In natural environments, bacteria often adhere to surfaces where they form complex multicellular communities. Surface adherence is determined by the biochemical composition of the cell envelope. We describe a novel regulatory mechanism by which the bacterium, Caulobacter crescentus, integrates cell...

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Main Authors: Aretha Fiebig, Julien Herrou, Coralie Fumeaux, Sunish K Radhakrishnan, Patrick H Viollier, Sean Crosson
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2014-01-01
Series:PLoS Genetics
Online Access:http://europepmc.org/articles/PMC3900383?pdf=render
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spelling doaj-4023feb1191144e280b7664eafc984582020-11-25T01:16:11ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042014-01-01101e100410110.1371/journal.pgen.1004101A cell cycle and nutritional checkpoint controlling bacterial surface adhesion.Aretha FiebigJulien HerrouCoralie FumeauxSunish K RadhakrishnanPatrick H ViollierSean CrossonIn natural environments, bacteria often adhere to surfaces where they form complex multicellular communities. Surface adherence is determined by the biochemical composition of the cell envelope. We describe a novel regulatory mechanism by which the bacterium, Caulobacter crescentus, integrates cell cycle and nutritional signals to control development of an adhesive envelope structure known as the holdfast. Specifically, we have discovered a 68-residue protein inhibitor of holdfast development (HfiA) that directly targets a conserved glycolipid glycosyltransferase required for holdfast production (HfsJ). Multiple cell cycle regulators associate with the hfiA and hfsJ promoters and control their expression, temporally constraining holdfast development to the late stages of G1. HfiA further functions as part of a 'nutritional override' system that decouples holdfast development from the cell cycle in response to nutritional cues. This control mechanism can limit surface adhesion in nutritionally sub-optimal environments without affecting cell cycle progression. We conclude that post-translational regulation of cell envelope enzymes by small proteins like HfiA may provide a general means to modulate the surface properties of bacterial cells.http://europepmc.org/articles/PMC3900383?pdf=render
collection DOAJ
language English
format Article
sources DOAJ
author Aretha Fiebig
Julien Herrou
Coralie Fumeaux
Sunish K Radhakrishnan
Patrick H Viollier
Sean Crosson
spellingShingle Aretha Fiebig
Julien Herrou
Coralie Fumeaux
Sunish K Radhakrishnan
Patrick H Viollier
Sean Crosson
A cell cycle and nutritional checkpoint controlling bacterial surface adhesion.
PLoS Genetics
author_facet Aretha Fiebig
Julien Herrou
Coralie Fumeaux
Sunish K Radhakrishnan
Patrick H Viollier
Sean Crosson
author_sort Aretha Fiebig
title A cell cycle and nutritional checkpoint controlling bacterial surface adhesion.
title_short A cell cycle and nutritional checkpoint controlling bacterial surface adhesion.
title_full A cell cycle and nutritional checkpoint controlling bacterial surface adhesion.
title_fullStr A cell cycle and nutritional checkpoint controlling bacterial surface adhesion.
title_full_unstemmed A cell cycle and nutritional checkpoint controlling bacterial surface adhesion.
title_sort cell cycle and nutritional checkpoint controlling bacterial surface adhesion.
publisher Public Library of Science (PLoS)
series PLoS Genetics
issn 1553-7390
1553-7404
publishDate 2014-01-01
description In natural environments, bacteria often adhere to surfaces where they form complex multicellular communities. Surface adherence is determined by the biochemical composition of the cell envelope. We describe a novel regulatory mechanism by which the bacterium, Caulobacter crescentus, integrates cell cycle and nutritional signals to control development of an adhesive envelope structure known as the holdfast. Specifically, we have discovered a 68-residue protein inhibitor of holdfast development (HfiA) that directly targets a conserved glycolipid glycosyltransferase required for holdfast production (HfsJ). Multiple cell cycle regulators associate with the hfiA and hfsJ promoters and control their expression, temporally constraining holdfast development to the late stages of G1. HfiA further functions as part of a 'nutritional override' system that decouples holdfast development from the cell cycle in response to nutritional cues. This control mechanism can limit surface adhesion in nutritionally sub-optimal environments without affecting cell cycle progression. We conclude that post-translational regulation of cell envelope enzymes by small proteins like HfiA may provide a general means to modulate the surface properties of bacterial cells.
url http://europepmc.org/articles/PMC3900383?pdf=render
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